• Biomolecules & Therapeutics
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• v.29 no.2
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• pp.227-233
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• 2021

Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon and ubiquitous environmental toxin with known harmful effects to human health. Abnormal phenotypes of keratinocytes are closely associated with their exposure to B[a]P. Resorcinol is a component of argan oil with reported anticancer activities, but its mechanism of action and potential effect on B[a]P damage to the skin is unknown. In this study, we investigated the effects of resorcinol on B[a]P-induced abnormal keratinocyte biology and its mechanisms of action in human epidermal keratinocyte cell line HaCaT. Resorcinol suppressed aryl hydrocarbon receptor (AhR) activity as evidenced by the inhibition of B[a]P-induced xenobiotic response element (XRE)-reporter activation and cytochrome P450 1A1 (CYP1A1) expression. In addition, resorcinol attenuated B[a]P-induced nuclear translocation of AhR, and production of ROS and pro-inflammatory cytokines. We also found that resorcinol increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activity. Antioxidant response element (ARE)-reporter activity and expression of ARE-dependent genes NAD(P)H dehydrogenase [quinone] 1 (NQO1), heme oxygenase-1 (HO-1) were increased by resorcinol. Consistently, resorcinol treatment induced nuclear localization of Nrf2 as seen by Western analysis. Knockdown of Nrf2 attenuated the resorcinol effects on ARE signaling, but knockdown of AhR did not affect resorcinol activation of Nrf2. This suggests that activation of antioxidant activity by resorcinol is not mediated by AhR. These results indicate that resorcinol is protective against effects of B[a]P exposure. The mechanism of action of resorcinol is inhibition of AhR and activation of Nrf2-mediated antioxidant signaling. Our findings suggest that resorcinol may have potential as a protective agent against B[a]P-containing pollutants.

• Korean Journal of Veterinary Research
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• v.60 no.4
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• pp.215-223
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• 2020

Sasa (S.) quelpaertensis Nakai (Korean name, Jeju-Joritdae), which has anti-oxidative and anti-inflammatory activities, is a type of bamboo grass distributed widely in Jeju Island, Korea. S. quelpaertensis leaves are used for therapeutic purposes in traditional Korean medicine. This study examined the hepatoprotective effects of the S. quelpaertensis ethyl acetate fraction (SQEA) in a mouse model to mimic alcoholic liver damage. The mice were administered orally with 30% alcohol (5 g/kg) once per day with or without SQEA treatments (100 and 200 mg/kg) for 14 days consecutively. Alcohol consumption increased the serum alcohol content and histopathological changes but reduced the liver weight. Moreover, the livers of the alcohol group exhibited the accumulation of malondialdehyde and cytochrome P450 2E1 (CYP2E1), and lipid droplet coating protein perilipin-2. On the other hand, SQEA dose-dependently attenuated the alcohol-induced serum ethanol content and liver histopathological changes but increased the liver weight. Moreover, SQEA attenuated the level of CYP2E1 and inhibited alcohol-induced lipogenesis in the liver via decreased perilipin-2 expression. These results suggest that SQEA can provide a potent way to reduce the liver damage caused by alcohol consumption.

• Journal of the Korean Society of Food Science and Nutrition
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• v.36 no.4
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• pp.411-418
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• 2007

Oxidative stress can play a key role in cadmium (Cd)-induced dysfunction. The present study examined the effect of pine needle water extract (PN) on Cd-induced oxidative stress in rats. Sprague-Dawley male rats were divided into three groups: normal group, Cd control group (Cd) and PN-administered Cd group (Cd-PN). $CdCl_2$ in 0.9% NaCl was administered orally with a dose of 5mg/kg of body weight/week, while the PN was administered orally with a dose of 1.26g/kg of body weight/day. Body weight gain was not different between groups, whereas food intakes were significantly lower in the Cd-PN group than in normal or Cd group. Relative liver weight was significantly increased by cadmium administration compared to the normal group. Hepatic cytochrome P450 was significantly lower in Cd and Cd-PN groups than in normal group, while xanthine oxidase and alcohol dehydrogenase activities were significantly higher in the Cd-PN group than in normal or Cd group. Increased hepatic superoxide dismutase, monoamine oxidase, catalase, and glutathione peroxidase activities by cadmium administration were significantly decreased by PN supplement. PN did not affect the hepatic glutathione content in cadmium-administered rats; however, PN significantly lowered the hepatic lipid peroxide level and plasma alanine transferase activity compared to the Cd control group. These results suggest that the PN may alleviate Cd-induced oxidative stress without hepatotoxicity.

• Journal of Life Science
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• v.20 no.1
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• pp.133-141
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• 2010

The protective effect of a mixed powder from solid-cultured and liquid-cultured Lentinus edodes mycelia (2:1, w/w) (designate LED) on the carbon tetrachloride ($CCl_4$)- and ethanol-induced hepatotoxicity of male Sprague-Dawley (SD) rat was investigated. In the $CCl_4$-induced rat hepatotoxicity experiment, rats of 4 groups (6 rats/group) were administere with Normal (0.2 ml distilled water), Control (0.2 ml distilled water), LED (LED 200 mg/kg BW + 0.2 ml distilled water), and Silymarin (200 mg/kg BW + 0.2 ml distilled water), p.o., daily for 2 weeks. Afterwards, all groups except for the Normal group were subjected to abdominal injection with $CCl_4$ ($CCl_4$ : corn oil, 1:1 v/v; 0.5 ml/kg BW). For the ethanol- induced rat hepatotoxicity experiment, rats were divided into 5 groups (5 rats/group): Normal; Pair-fed control (PFC); Control (ethanol); LED (ethanol + LED 200 mg/kg BW); and Silymarin (ethanol + silymarin 200 mg/kg BW). Rats of the Normal and PFC groups were fed a basal liquid diet, and rats of the Control, LED, and Silymarin groups were fed a liquid ethanol diet containing LED or Silymarin. Eight weeks later, blood and liver samples were collected to analyze biomarkers. In $CCl_4$-induced SD rats, LED elevated hepatic superoxide dismutase (SOD), catalase, and glutathione peroxidase (GSH peroxidase) activities and thiobarbituric reactive substances (TBARS) were reduced, resulting in the reduction of glutamate-oxalate transaminase (GOT), glutamate-pyruvate transaminase (GPT) and lactic dehydrogenase (LDH) activities in plasma. Similar results of these enzymes and biochemical markers in both liver tissues and plasma were seen in ethanol-induced hepatotoxicity of SD rats. In addition, elevated alcohol dehydrogenase (ADH) activity and reduced expression of cytochrome p450 mixed monooxygenase enzyme (CYP2E1) were seen in liver tissues from ethanol-treated rats by LED treatment. These effects of LED were similar to those of Silymarin. In in vitro experiments, LED showed antioxidant activity in a 2,2-diphenyl-1-picrylhydrazyl (DPPH) system and mouse liver mitochondria system induced by NADPH/$Fe^{2+}$ and cumine hydroperoxide (CuOOH). These results indicate that LED protected SD rat hepatotoxicity, induced by $CCl_4$ and ethanol, through its antioxidative activity and might be useful as a material for protection from hepatoxicity in humans.